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A Common Complication of Prolonged Therapy: A Report of Eight Cases

Gillian C. Hawthorne, MB, MRCP; Norman P. S. Campbell, MD, MRCP; John S. Geddes, BSc, MD, FRCP, FACC; W. Rodney Ferguson, MSc, PhD; William Postlethwaite, FIMLS, MSc; Brian Sheridan, BA, MSc; A. Brew Atkinson, BSc, MD, MRCP

Arch Intern Med. 1985;145(6):1016-1019.

Abstract
• Amiodarone is a widely used antiarrhythmic drug, which contains 75 mg of iodide per 200 mg of active substance. Eight of our patients receiving long-term amiodarone therapy became hypothyroid. Seven of these patients had no previous history of thyroid dysfunction or goiter. Antithyroid antibodies were absent, and standard perchlorate discharge tests were positive in seven patients when hypothyroidism was diagnosed. In one patient, amiodarone therapy was withdrawn; over the next nine months, the hypothyroidism resolved, and results of the perchlorate discharge test reverted to normal. We conclude that amiodarone-induced hypothyroidism is similar to previously described iodide-induced hypothyroidism. It may develop in the absence of a previous history of thyroid disease, and all patients receiving long-term amiodarone therapy should therefore be regularly monitored for hypothyroidism.

(Arch Intern Med 1985;145:1016-1019)

Author Affiliations
From the Sir George E. Clark Metabolic Unit (Drs Hawthorne and Atkinson), the Regional Medical Cardiology Centre (Drs Campbell and Geddes), the Regional Endocrine Laboratory (Drs Postlethwaite and Sheridan), and the Regional Medical Physics Service (Dr Ferguson), Royal Victoria Hospital, Belfast.

Footnotes
Accepted for publication Sept 21, 1984.

Reprint requests to the Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Grosvenor Rd, Belfast, BT12 6BA, Northern Ireland (Dr Atkinson).

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